Failure of itraconazole to prevent Enterocytozoon bieneusi infection.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to H Albrecht.
Explore the source record for details and available documents.
BACKGROUND: A wide variety of bacterial, viral, and parasitic pathogens can cause severe diarrhea in patients with advanced human immunodeficiency virus (HIV) infection. Conflicting evidence exists as to whether Blastocystis hominis should also be included among the infectious agents capable of causing HIV-related diarrhea. METHODS: We determined the prevalence and clinical significance of B. hominis in a cohort of 262 patients with HIV infection, presenting at the infectious diseases department of a tertiary referral university hospital in northern Germany. RESULTS: B. hominis was detected in stool samples of 99 patients (38%). The isolation rate varied highly between the different groups. Homosexual men (43%; odds ratio (OR), 2.1; p = 0.01) had a higher detection rate than patients from other risk groups (26%), and patients with acquired immunodeficiency syndrome (46%; OR, 1.8; p = 0.03) were more likely to carry B. hominis than patients in earlier stages of their HIV infection (32%). An association with clinical symptoms was not evident. Presence of B. hominis, however, was frequently associated with the concurrent isolation of other enteric pathogens or apathogenic parasites. CONCLUSIONS: The data suggest that the isolation of B. hominis does not justify treatment even in symptomatic, severely immunocompromised patients. Most patients will either have spontaneous resolution of symptoms or successful identification of other infectious or noninfectious etiologies. Therapy should be limited to patients with persistent unexplained symptoms after a thorough evaluation and a complete screening for alternative etiologies, including the use of endoscopic procedures and the careful examination of multiple specimens.
Between June 1986 and October 1992, disseminated toxoplasmosis was diagnosed in 16 AIDS patients. 13 cases were diagnosed at autopsy where multiple organ involvement was documented in all 13. Three patients were diagnosed intra vitam. All 3 survived with appropriate treatment. Clinical features indicative of disseminated toxoplasmosis were: fever of unknown origin between 39 degrees and 40 degrees C in 16 cases, clinical signs suggestive of sepsis or septic shock in 15, with progression to multiorgan failure in 10, disseminated intravascular coagulopathy in 6, confusion, disorientation or apathy in 13 and lack of a systemic pneumocystis carinii prophylaxis in all 16. Typical laboratory markers were: CD4 cell counts below 100 x 10(6)/l in 16 cases, elevation of serum lactic dehydrogenase in 16 and creatine phosphokinase (in 4/6), normal or only slightly elevated C-reactive protein (in 9/11), positive Toxoplasma gondii IgG antibodies in 15/16 and negative IgM antibodies in all 16. Lesions indicative of cerebral toxoplasmosis were visualized on cranial computerized tomography in only 3/10 evaluated patients. In patients with advanced HIV infection presenting with a systemic illness, including the clinical and laboratory features described above, systemic Toxoplasma gondii infection must be included in the differential diagnosis. In these patients, specific and if warranted, invasive diagnostic procedures followed by early vigorous therapeutic intervention should be considered.
Previous work on the transcriptional regulation of the mouse TNF-alpha promoter had indicated a major role for the NF-kappa B transcription factor in the induction of the gene by endotoxin. However, similar studies using the human promoter failed to establish a role for this factor. We measured the nuclear migration of NF-kappa B and the accumulation of TNF-alpha mRNA in murine T lymphoblasts and bone marrow-derived macrophages (BMDM) under different activation conditions, seeking to establish a correlation. Activation of NF-kappa B and accumulation of TNF-alpha mRNA correlated semiquantitatively under the following conditions: (1) inhibition of NF-kappa B by dithiocarbamates; (2) induction of TNF synthesis by taxol; (3) partial induction of TNF-alpha mRNA by various inducers in macrophages from lpsd mice; and (4) inhibition of NF-kappa B activation by a protease inhibitor. However, inhibition of TNF-alpha mRNA accumulation by cAMP inducers had no effect on NF-kappa B induction. We conclude that NF-kappa B translocation is necessary, but not sufficient for the transcriptional induction of the TNF-alpha gene by LPS in macrophages or by phorbol ester and ionomycin in T lymphocytes.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The recent demonstration of the anti-oxidant properties of the Bcl-2 gene product suggested that expression of Bcl-2 may interfere with the nuclear migration of the NF-kappa B transcription factor, which is thought to depend on the presence of reactive oxygen intermediates. In mouse L cells, overexpression of Bcl-2 interfered with the activation of NF-kappa B by H2O2. However, Bcl-2 had no effect on the activation of NF-kappa B by TNF, even though it protected cells from TNF-induced apoptosis. The effects of exogenous pyrrolidine dithiocarbamate were very similar to those of Bcl-2 overexpression. We conclude that the protective effects of anti-oxidants against induced apoptotic cell death are unrelated to their ability to interfere with NF-kappa B activation.
A 41-year-old man infected with HIV-1 developed fever up to 39.8 degrees C together with nonproductive cough and dyspnoea. Lactate dehydrogenase concentration rose from a level of 998 U/l to 6307 U/l. As pneumocystis carinii pneumonia was at first suspected he was treated with co-trimoxazole (1600 mg sulfamethoxazole and 320 mg trimethoprim, four times daily). But the symptoms did not abate. Bone-marrow puncture revealed numerous macrophages containing ovoid inclusions typical of Histoplasma capsulatum varietas capsulatum. The diagnosis of disseminated histoplasmosis was confirmed by culture and serologically by an increase in Histoplasma polysaccharide antigen. On treatment with amphotericin B (at first 10 mg, then 50 mg daily for 4 weeks) the symptoms regressed within a few days. After the concentrations of lactate dehydrogenase and Histoplasma antigen had become normal again, maintenance treatment was changed to itraconazole (200 mg twice daily), after a total amphotericin B dose of 1150 mg. The patient has remained free of recurrence.
BACKGROUND: We report on a retrospective study in 544 HIV-positive patients, (42 women, 502 men, mean age 35 years) showing CD4 lymphocyte counts below 200 c/mcl or after their cure of Pneumocystis carinii pneumonia, who received 300 mg pentamidine aerosol as prophylaxis against Pneumocystis carinii pneumonia every four week. PATIENTS AND METHODS: 277 patients were asymptomatic, 120 in the AIDS related complex stage (ARC) and 147 in the full stage of AIDS. The mean follow-up was 14.4 months. RESULTS: A total of 25 cases of Pneumocystis carinii pneumonia was observed (3.83/year): in the primary prophylaxis group 18 (3.25%/year), in the secondary prophylaxis group seven (6.8%/year). By introducing the loading dose (one inhalation per day for five consecutive days for patients with CD4 cell counts below 150 c/mcl) we reduced the percentage of early manifestations within the first three months from 61% to 14%. No extrapulmonary Pneumocystis carinii manifestation was observed. CONCLUSION: This study supports the efficacy of pentamidine aerosol prophylaxis of primary and secondary Pneumocystis carinii pneumonia.
It is well known that bacterial lipopolysaccharide (LPS) induces the synthesis of tumor necrosis factor alpha (TNF-alpha) and other inflammatory cytokines by primary monocytes and macrophages and that the Th1 lymphokines, interleukin-2 (IL-2) and interferon-gamma (IFN-gamma), augment this response. We investigated the ability of IL-2 and IFN-gamma to induce the production of TNF-alpha mRNA and protein independently of LPS and the modulation of this response by macrophage colony-stimulating factor (M-CSF) and IL-10. We found that IL-2 and IFN-gamma were both able to induce the accumulation of TNF-alpha mRNA, albeit with slower kinetics than LPS, and that they acted synergistically. However, very little TNF bioactivity was secreted by lymphokine-stimulated macrophages unless LPS was also added. This finding underscores the importance of translational effects in the control of TNF production. M-CSF and IL-10 strongly inhibited TNF production at the level of both mRNA and bioactivity but had no effect on the production of IL-6. Bone marrow-derived or thioglycollate-elicited macrophages from the NZW mouse strain, which have been reported to be deficient in their ability to produce TNF, were at least as responsive to LPS or lymphokines as those taken from the C57Bl/6 strain and were similarly affected by M-CSF and IL-10. Therefore, the genetic defect of NZW mice is not a primary deficiency in TNF production.
The case of a 33-year-old patient with rapid onset of bilateral parotid gland and lymph node abscesses is described. The patient was positive for human immunodeficiency virus 1 and presented with a history of interstitial lymphocytic pneumonia and pneumococcal meningitis prior to admission. The patient received cotrimoxazole as primary prophylaxis against Pneumocystis carinii pneumonia. Fine needle aspiration from the abscesses yielded Streptococcus pneumoniae. Penicillin G treatment in combination with surgical drainage of the lesions led to healing with minimal residual lymph node enlargement. No relapse was noted until 12 months after presentation.
Visceral leishmaniasis (kala-azar) affecting HIV-infected patient is being reported in increasing frequency. A 40-year-old German bisexual patient with full-blown AIDS is described who presented with Kaposi's sarcoma, epigastric pain, diarrhea, and weight loss but without fever. Leishmania amastigotes were initially found in biopsies from stomach, duodenum, and a cutaneous Kaposi's sarcoma lesion but were later also recovered from bone marrow and lymph node. The patient received three courses of a combination of pentavalent antimony and interferon-gamma. In addition to the common side effects such as fever, thrombocytopenia, and elevated amylase and lipase, a vivid progression of the Kaposi's sarcoma was noted. Tumor progression was temporally closely associated with treatment with interferon-gamma. Because this phenomenon has also been observed in other patients, we advise caution when using interferon-gamma in patients with Kaposi's sarcoma.
Central nervous system disease due to Toxoplasma gondii is a common cause of morbidity and mortality in patients with the acquired immunodeficiency syndrome. Cardiac toxoplasmosis, however, has been described in only a limited number of cases. In a 45-year-old patient with symptoms suggestive of myocarditis, Toxoplasma gondii was detected in myocardial tissue obtained by biopsy. After the institution of appropriate antiprotozoal therapy, the patient recovered. This patient is believed to be the first patient to survive biopsy-proven myocarditis caused by Toxoplasma gondii. Cardiac toxoplasmosis should be ruled out in HIV-infected patients presenting with high fever and/or cardiorespiratory symptoms and exhibiting serologic evidence of prior exposure to Toxoplasma gondii as determined by a positive IgG EIA, especially if the CD4+ count is low and no systemic Pneumocystis carinii pneumonia prophylaxis has been administered. A high index of clinical suspicion and, if necessary, invasive diagnostic tests, including myocardial biopsies, are most important in making the correct diagnosis.
The development of the visual cortex was studied in 30 Trisomy 19 (Ts19) mice aged 1-16 days postpartum and their euploid littermates. Morphogenesis of the Ts19 visual cortex, though delayed in development, followed the regular sequence observed in control littermates. Early morphogenetic events, such as obliteration of the ventricular lumen, disappearance of the ventricular zone, formation of a visible apical dendrite, as well as disappearance of both migrating neurons and the columnar organization of bipolar preneurons were delayed by 1 day; maturation steps occurring later such as appearance and disappearance of perikaryal basophilia were delayed by 2 days. Myelination of the white matter was similarly retarded by 2 days. The fronto-occipital length of the cerebral hemispheres and the thickness of the visual cortex were decreased by about 20%, consistent with a hypoplasia of the Ts19 neocortex. Unlike in the cerebral cortex of human Ts21, morphometric analysis of the visual cortex of Ts19 mice did not give any indication of a selective deficit in a particular neuron population; the increased cell density and the reduced nuclear volume observed during early postnatal development are attributable to a maturational delay. The relevance of these results with respect to the mechanisms underlying neuropathological alterations in human Ts21 is discussed.
OBJECTIVE: To assess the natural history of Kaposi's sarcoma (KS) in HIV-positive women living in Germany. METHODS: All physicians reporting the diagnosis of KS in a female patient were contacted and asked for detailed information. DESIGN: Descriptive study of clinical, epidemiological and immunological data of ten women with biopsy-proven KS living in Germany were evaluated. The results are compared with those of other previously published studies of women with KS from Italy, France and the USA. SETTING: Five centres in Germany. RESULTS: Of 765 German women with AIDS, only 10 (1.3%) were reported to suffer from Kaposi's sarcoma (KS) compared with 1771 of 8128 men (21.8%). Mean age in these women was 39.7 years. KS was the first AIDS defining event in nine women and the reason for HIV-testing in three. The mean CD4 count was 215/microliters. Two patients were of African origin, had only recently come to Germany and were most likely to have acquired their HIV-infection in Africa. Three patients were i.v.-drug users (IVDU). Two of these (and most likely all three) had worked as prostitutes. Of five women who had contracted HIV via heterosexual contacts, one worked as a prostitute and the other four were married to or were living together with a bisexual HIV-positive man. All four male partners have also developed KS. The course of the disease seems to be particularly aggressive in female patients with eight of 10 women presenting with or progressing to widely disseminated disease with extensive involvement of internal organs. In this cohort survival was longer in females who acquired their HIV infection heterosexually compared to IVDU and was strongly correlated with higher CD4-counts at diagnosis. CONCLUSIONS: KS seems to run a particularly aggressive course in women. Our data are consistent with a sexually transmittable aetiological agent of KS. Prostitution, an issue yet to be addressed by other authors reporting series of women with KS, was reported in four of our patients. Further studies are needed to clarify the significance of this finding.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.